Stent-supported reconstruction of the aortoiliac bifurcation with the kissing balloon technique.
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BACKGROUND: Bilateral iliac artery obstructions involving the aortic bifurcation or high-grade stenosis of the abdominal aorta are not usually considered an indication for percutaneous treatment. The purpose of the present study was to evaluate the initial and long-term results of primary stent implantation for reconstruction of the aortic bifurcation. METHODS AND RESULTS: In 48 patients with obstructions of the aortoiliac segment, primary stent implantation was performed with the "kissing balloon technique." Preinterventional angiography showed bilateral stenoses (>85%) of the proximal common iliac arteries in 25 patients, unilateral occlusions and contralateral stenosis in 22 patients, and bilateral occlusion in 1 patient. In 7 cases, stents were placed for the treatment of high-grade infrarenal aortic stenoses. After excimer laser-assisted recanalization of the common iliac artery obstructions, the aortic bifurcation was reconstructed with the bilateral simultaneous implantation of Palmaz stents (diameter, 7 to 8 mm). Stents used for the treatment of aortic stenoses (Palmaz, n=6; Gianturco, n=1) had a diameter ranging from 20 to 25 mm. In all patients, stents were placed successfully (residual stenosis <30%) and without complications. A clinical improvement of +2 to +3 according to American Heart Association criteria was observed in 41 and 7 patients, respectively. Follow-up was performed clinically (standardized treadmill testing and color-coded Doppler ultrasound) and angiographically. The primary angiographic patency rate (24-month follow-up) was 86.8%. In 3 patients, angiography revealed significant restenoses, which were successfully treated with percutaneous transluminal angioplasty. CONCLUSIONS: Primary stent implantation with the kissing balloon technique is safe and effective for the treatment of aortoiliac obstructions involving the aortic bifurcation and represents a true endovascular alternative to surgery. (+info)
Effect of pulmonary edema on tracheal diameter.
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BACKGROUND: Though it is well known that cardiogenic and noncardiogenic pulmonary edema can cause changes in lung mechanics, actual alterations in tracheal diameter have not been described. OBJECTIVE: To evaluate the effects of pulmonary edema induced by increased left atrial pressure (cardiogenic) and Perilla ketone (PK; noncardiogenic) on tracheal diameter in chronically instrumented awake sheep. METHODS: We investigated the effects of two mechanistically distinct types of pulmonary edema on tracheal diameter in chronically instrumented awake sheep. Cardiogenic pulmonary edema (analogous to congestive heart failure in humans) was induced by increasing left atrial pressure ( upward arrowP(LA)) by inflating the balloon on a Foley catheter positioned in the mitral valve annulus to cause partial obstruction to flow across the valve (n = 18). Noncardiogenic pulmonary edema (increased pulmonary microvascular permeability pulmonary edema analogous to the acute respiratory distress syndrome in humans) was produced by the intravenous administration of PK (n = 11). Lateral chest radiographs (CXRs) were scored by a standardized 5-point scoring system for the severity of pulmonary edema, and tracheal diameter was measured at a fixed location in the carina. Three radiologists, blinded to sheep identification number and experimental protocol, evaluated the radiographs independently at different points in time for edema severity and tracheal diameter. The sheep were sacrificed immediately after the final CXR, and wet/dry lung weight ratio (W/D ratio) was determined. RESULTS: Both upward arrowP(LA) and PK were associated with statistically significant tracheal narrowing ( upward arrowP(LA): 20.3 +/- 0.6 to 15.1 +/- 0.9 mm; PK: 20.2 +/- 0.6 to 14.1 +/- 1.4 mm). Tracheal narrowing correlated with the severity of the pulmonary edema determined radiographically ( upward arrowP(LA): r = -0.69, p < 0.01; PK: r = -0.62, p < 0.01) and by W/D ratio ( upward arrowP(LA): r = -0.64, p < 0.05; PK: r = -0.54, p < 0. 05). CONCLUSIONS: We conclude that tracheal narrowing occurs in sheep models of both cardiogenic and noncardiogenic pulmonary edema and that the degree of narrowing correlates with the severity of the edema. (+info)
Frequency of early occlusion and stenosis in a left internal mammary artery to left anterior descending artery bypass graft after surgery through a median sternotomy on conventional bypass: benchmark for minimally invasive direct coronary artery bypass.
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BACKGROUND: Uncertainty exists regarding the frequency of early occlusion when the left internal mammary artery (LIMA) is anastomosed to the left anterior descending artery (LAD) through a sternotomy with conventional coronary artery bypass grafting (CABG). The issue has gained importance for comparison with less invasive surgical approaches in which operative exposure may be limited and graft anastomosis more difficult. METHODS AND RESULTS: Data were analyzed from the International Multicenter Aprotinin Graft Patency Experience (IMAGE) trial in which 617 patients underwent conventional CABG of the LAD with a LIMA between April 1993 and May 1995. Coronary angiography was performed a mean of 10.8 days postoperatively. Patients were randomized to receive intraoperative aprotinin, an inhibitor of several serine proteinases, or placebo. Because no differences existed in patency rates of LIMA grafts between patients who received aprotinin and placebo, both groups were analyzed collectively. On coronary angiography, the LIMA was widely patent (<50% stenosis) in 561 patients (91%), had > or = 50% and <99% stenosis in 48 patients (7.8%), and was occluded in 8 patients (1.3%). Therefore, the LIMA was patent in 609 patients (98.7%). Conclusions-In the IMAGE trial, the largest and most contemporary early angiographic analysis of CABG available, early patency of the LIMA was >98% when anastomosed to the LAD. These data provide an important benchmark for less invasive surgical approaches in which the LIMA is anastomosed to the LAD. (+info)
Profound apoptosis-mediated regional myocyte loss and compensatory hypertrophy in pigs with hibernating myocardium.
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BACKGROUND: Myocyte apoptosis is seen in ischemic heart disease, but whether it can occur after reversible ischemia or independent of necrosis and replacement fibrosis is unknown. METHODS AND RESULTS: Pigs were instrumented with a stenosis of the left anterior descending coronary artery to chronically reduce coronary flow reserve over a period of 3 months. At this time, there was viable dysfunctional myocardium having the physiological features of hibernating myocardium. Resting subendocardial perfusion was reduced to 0.65+/-0.08 (mean+/-SEM) mL. min(-1). g(-1) in hibernating myocardium of instrumented pigs compared with 0.98+/-0.14 mL. min(-1). g(-1) in myocardium of sham-operated pigs (P<0.05). There was a critical limitation in subendocardial flow during vasodilation to 0.78+/-0.20 mL. min(-1). g(-1) in instrumented pigs versus 3. 24+/-0.50 mL. min(-1). g(-1) in sham-operated pigs (P<0.001). Histology revealed a regional reduction in myocyte nuclear density to 995+/-100 nuclei/mm(2) in hibernating myocardium from the instrumented group versus 1534+/-65 nuclei/mm(2) in myocardium from the sham-operated group (P<0.05), regional myocyte hypertrophy (myocyte volume per nucleus, 14 183+/-2594 in the instrumented group versus 9130+/-1301 microm(3) in the sham group; P<0.05), and minimal increases in connective tissue (5.8+/-0.9% in the instrumented group versus 3.0+/-0.2% in the sham group, P<0.05). Necrosis was not identified, but apoptosis was increased from 30+/-9 myocytes per 10(6) myocyte nuclei in myocardium from the sham group to 220+/-77 myocytes per 10(6) myocyte nuclei in hibernating myocardium (P<0.05). CONCLUSIONS: These findings indicate that reversible ischemia in an area of chronically reduced coronary flow reserve induces regional myocyte loss via an apoptotic mechanism. This may contribute to the progression of chronic coronary disease to heart failure and explain the lack of complete functional recovery after revascularization in hibernating myocardium. (+info)
Accelerated neointima formation after vascular injury in mice with stromelysin-3 (MMP-11) gene inactivation.
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The hypothesis that stromelysin-3 (MMP-11), a unique member of the matrix metalloproteinase (MMP) family, plays a role in neointima formation was tested with the use of a vascular injury model in wild-type (MMP-11(+/+)) and MMP-11-deficient (MMP-11(-/-)) mice. Neointima formation 2 to 3 weeks after electric injury of the femoral artery was significantly enhanced in MMP-11(-/-) as compared with MMP-11(+/+) mice, in both mice of a pure 129SV genetic background (0.014 versus 0.0010 mm(2) at 2 weeks, P<0.001) and those of a 50/50 mixed 129SV/BL6 background (0.030 versus 0.013 mm(2) at 3 weeks, P<0.05). The medial areas were comparable, resulting in intima/media ratios that were significantly increased in MMP-11(-/-) as compared with MMP-11(+/+) arteries, in mice of both the 129SV (1. 0 versus 0.18, P<0.001) and mixed (1.5 versus 0.70, P<0.05) backgrounds. Nuclear cell counts in cross-sectional areas of the intima of the injured region were higher in arteries from MMP-11(-/-) mice than in those from MMP-11(+/+) mice (210 versus 48, P<0.001, in pure 129SV mice and 290 versus 150, P<0.01, in mice of the mixed genetic background). Immunocytochemical analysis revealed that alpha-actin-positive and CD45-positive cells were more abundant in intimal sections of MMP-11(-/-) mice. Degradation of the internal elastic lamina was more extensive in arteries of MMP-11(-/-) mice than in those of MMP-11(+/+) mice (39% versus 6.8% at 3 weeks, P<0. 005). The mechanisms by which MMP-11 could impair elastin degradation and cellular migration in this model remain, however, unknown. (+info)
Calcineurin plays a critical role in pressure overload-induced cardiac hypertrophy.
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BACKGROUND: Cardiac hypertrophy is a fundamental adaptive response to hemodynamic overload; how mechanical load induces cardiac hypertrophy, however, remains elusive. It was recently reported that activation of a calcium-dependent phosphatase, calcineurin, induces cardiac hypertrophy. In the present study, we examined whether calcineurin plays a critical role in pressure overload-induced cardiac hypertrophy. METHODS AND RESULTS: Pressure overload produced by constriction of the abdominal aorta increased the activity of calcineurin in the rat heart and induced cardiac hypertrophy, including reprogramming of gene expression. Treatment of rats with a calcineurin inhibitor, FK506, inhibited the activation of calcineurin and prevented the pressure overload-induced cardiac hypertrophy and fibrosis without change of hemodynamic parameters. Load-induced expression of immediate-early-response genes and fetal genes was also suppressed by the FK506 treatment. CONCLUSIONS: The present results suggest that the calcineurin signaling pathway plays a pivotal role in load-induced cardiac hypertrophy and may pave the way for a novel pharmacological approach to prevent cardiac hypertrophy. (+info)
Coronary dissection due to overdilatation of an elastic membrane of the multi-link stent delivery system caused by balloon rupture.
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A 65-year-old male with unstable angina underwent coronary angiography, which revealed a significant stenotic lesion in the right coronary artery. This narrowing was subsequently treated with the Multi-Link stent. During the balloon inflation associated with stent deployment, balloon rupture occurred and resulted in overdilatation of an elastic membrane in the stent delivery system. This, in turn, resulted in coronary dissection, which required treatment with further stenting. (+info)
Carvedilol and lacidipine prevent cardiac hypertrophy and endothelin-1 gene overexpression after aortic banding.
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Carvedilol and lacidipine have been shown to exert cardioprotective effects in rat models of chronic hypertension. We investigated their effects in an acute model of pressure overload produced by suprarenal aortic constriction, in which enhanced myocardial production of endothelin-1 could play a crucial role. In the absence of drug treatment, after 1 week, aortic banding provoked an increase in carotid pressure associated with left ventricular hypertrophy (29%; P<0.01). These changes were accompanied by increased myocardial expression of preproendothelin-1 (2.5 times; P<0.05) and skeletal alpha-actin (3.6 times; P<0.05), but the expression of cardiac alpha-actin was not modified. Oral administration of carvedilol at a dose of 30 mg. kg(-1). d(-1) to rats with aortic banding normalized carotid pressure and left ventricular weight as well as preproendothelin-1 and skeletal alpha-actin gene expression. Carvedilol at a lower dose (7.5 mg x kg(-1) x d(-1)) and lacidipine 1 mg x kg(-1) x d(-1) had only moderate and nonsignificant effects on carotid pressure but largely prevented left ventricular hypertrophy (P<0.01) and preproendothelin-1 overexpression (P<0.05). Labetalol (60 mg x kg(-1) x d(-1)) tended to exert similar effects but insignificantly. These results show that the antihypertrophic properties of carvedilol and lacidipine are partly independent of their antihypertensive effects and may be related to their ability to blunt myocardial preproendothelin-1 overexpression. Moreover, carvedilol at a dose of 7.5 mg x kg(-1) x d(-1) did not prevent myocardial overexpression of skeletal alpha-actin, which suggests that, in this model, reexpression of a fetal gene can be activated by pressure overload independently of cardiac hypertrophy. (+info)